期刊
EXPERIMENTAL GERONTOLOGY
卷 113, 期 -, 页码 209-217出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2018.10.005
关键词
Aging; D-galactose; Sodium butyrate; Histone deacetylases; DNA damage
资金
- CAPES, Brazil
- CNPq, Brazil
- FAPESC, Brazil
- UNESC, Brazil
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - Brasil (CAPES) [001]
- CNPq [312184/2016-6]
Aging is a complex biological process. Epigenetic alterations have been related to both aging and memory decline. Included amongst these alterations is histone acetylation, which may play a crucial role in aging. Thus, the aims of the present study were to standardize the animal model of D-galactose (D-gal), and to evaluate the effects caused by sodium butyrate (SB), which is a histone deacetylase inhibitor on memory, the modulation of histone deacetylases (HDACs), and also DNA damage in 2, 6 or 16-month-old Wistar rats which were subjected to administrations of D-gal. To help choose the best dose of D-gal for the induction of the aging model, we performed a dose-response curve (100, 200 or 300 mg/kg). D-Gal was administered orally to the 2-month-old rats for a period of 30 days. After this, D-gal (200 mg/kg) or water were administered to the 2, 6 or 16-month-old rats for a period of 30 days. On the 24th day, treatment was started with SB (600 mg/kg) intraperitoneally, for a period of 7 days. SB was able to reverse the damage to habituation memory caused by D-gal in the 2 and 6-month-old rats, but was unable to reverse the damage in the 16 month-old animals. In addition, SB was able to reverse the damage caused by natural aging in the 16-month-old animals. In the inhibitory avoidance task, SB improved the damage caused by D-gal in the 2, 6 and 16-month-old animals and had the same result against the effects of natural aging in the 16-month-old rats. Moreover, D-gal caused an increase in the level of HDACs activity in the 16-month-old animals, and SB was able to reverse this effect in the frontal cortex and hippocampus. The 16-month-old animals showed an increase in the frequency of DNA damage in peripheral blood, and SB was able to reduce this damage. Moreover, D-gal caused an increase in the index and frequency of DNA damage in the 2 and 6-month-old animals, and treatment with SB was able to prevent this damage. Thus, the present study showed the protective effects of SB on the memory of naturally aged and D-gal induced aging in rats. Therefore, the present study shows new findings for the use of SB in aging.
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